Advancing brain tumor detection: harnessing the Swin Transformer's power for accurate classification and performance analysis.

The accurate detection of brain tumors through medical imaging is paramount for precise diagnoses and effective treatment strategies. In this study, we introduce an innovative and robust methodology that capitalizes on the transformative potential of the Swin Transformer architecture for meticulous brain tumor image classification. Our approach handles the classification of brain tumors across four distinct categories: glioma, meningioma, non-tumor, and pituitary, leveraging a dataset comprising 2,870 images. Employing the Swin Transformer architecture, our method intricately integrates a multifaceted pipeline encompassing sophisticated preprocessing, intricate feature extraction mechanisms, and a highly nuanced classification framework. Utilizing 21 matrices for performance evaluation across all four classes, these matrices provide a detailed insight into the model's behavior throughout the learning process, furthermore showcasing a graphical representation of confusion matrix, training and validation loss and accuracy. The standout performance parameter, accuracy, stands at an impressive 97%. This achievement outperforms established models like CNN, DCNN, ViT, and their variants in brain tumor classification. Our methodology's robustness and exceptional accuracy showcase its potential as a pioneering model in this domain, promising substantial advancements in accurate tumor identification and classification, thereby contributing significantly to the landscape of medical image analysis.

A systematic review of the associations between sedentary behavior, physical inactivity, and non-motor symptoms of Parkinson's disease.

BACKGROUND: Parkinson's disease (PD), known for motor symptoms, often presents early non-motor issues that significantly affect patients' quality of life. While effective treatments are limited, physical activity and exercise offer potential benefits. However, an overlooked aspect of the movement intensity continuum is prolonged sitting or sedentary behavior, and physical inactivity. Thus, this study aimed to conduct a systematic review investigating the associations between sedentary behavior, physical inactivity, and non-motor symptoms, specifically cognitive impairment, depression, and poor sleep in PD. METHODS: Conforming to PRISMA guidelines, a systematic search of the literature was conducted via electronic databases including MEDLINE, CINAHL, Scopus, PubMed and PsycINFO up to February 28, 2023. Studies were included if they investigated associations between sedentary behavior or physical inactivity and at least one non-motor symptom such as depression, poor sleep, and/or cognitive impairment, in adults aged 18 years or older with PD. Quality assessment of the studies was performed using the Newcastle-Ottawa scale for cross-sectional and cohort studies. RESULTS: Of the 463 publications found, 7 studies met the inclusion criteria (n = 980 unique participants). Sample sizes ranged from 17 to 487 participants, and all studies were observational, conducted in home or community settings. Collectively, these studies show that higher amounts of both objectively-measured and self-reported sedentary time are associated with worse scores on standardized measures of cognition and the Parkinson's Disease Questionnaire (PDQ) summary index and its subscales, such as cognition (memory and concentration). Additionally, longitudinal cohort studies suggest that physical inactivity and higher sedentary behavior are associated with depression and cognitive impairment in PD. Less sleep was associated with higher sedentary behavior. CONCLUSION: Associations observed between physical inactivity, sedentary behavior, and non-motor symptoms in PD underscore the need to address these factors for enhanced well-being. Further well-designed studies are essential to assess the impact of reducing sedentary behavior and physical inactivity on non-motor symptoms in PD. Prospero registration number: PROSPERO (ID: CRD42023405422) on April 11, 2023.

The whole day matters after stroke: Study protocol for a randomized controlled trial investigating the effect of a 'sit less, move more, sleep better' program early after stroke.

BACKGROUND: Movement-related behaviours, including prolonged sedentary behaviour, physical inactivity, and poor sleep, are associated with worse functional outcomes poststroke. Addressing these co-dependent behaviours early after stroke may help to optimize recovery and improve overall quality of life for individuals with stroke. OBJECTIVE: This study aims to determine the feasibility and effect of a 'sit less, move more, sleep better' program early after stroke on functional mobility and global disability outcomes, while also exploring imaging and behavioural markers that may influence walking recovery. METHODS: The study is an assessor-blinded, single-center, parallel-group, randomized controlled trial to be completed within 24 months from July 12, 2023 to June 30, 2025. We will enroll 50 patients with acute ischemic stroke within 7 days from symptom onset, aged 18 years or older, and with ongoing walking goals. Demographic and stroke characteristics, including stroke risk factors, neuroimaging, and acute stroke treatments, will be determined and documented. All participants will wear an accelerometer for one week at three different time-points (baseline, 6, and 12 weeks) to assess movement-related behaviours. Following randomization, participants in the intervention arm will receive a 'sit less, move more, sleep better' program for up to 1 hour/day, 5 days/week, for 6 weeks to enhance self-efficacy for change. Participants in the control arm will receive usual inpatient and early supported stroke discharge care. The feasibility outcomes will include reach (enrolled/eligible), retention (completed/enrolled), adverse events, and program adherence. Other outcomes at 6 and 12 weeks include the modified Rankin Scale, Timed-Up and Go, movement-related behaviours, walking endurance, gait speed, cognition, stroke severity and quality of life. Mixed-effects models will assess changes in outcomes over time. Compositional associations between movement-related behaviours and outcomes will consider covariates such as imaging markers. DISCUSSION: Adopting a whole-day approach to poststroke rehabilitation will provide valuable insights into the relationship between optimizing movement-related behaviours early after stroke and their impact on functional outcomes. Through exploring person-specific behavioural and imaging markers, this study may inform precision rehabilitation strategies, and guide clinical decision making for more tailored interventions. TRIAL REGISTRATION: Clinical Trial registration (ClinicalTrials.gov Identifier: NCT05753761, March 3, 2023).

NEU1-A Unique Therapeutic Target for Alzheimer's Disease.

Neuraminidase 1 (NEU1) is considered to be the most abundant and ubiquitous mammalian enzyme, with a broad tissue distribution. It plays a crucial role in a variety of cellular mechanisms. The deficiency of NEU1 has been implicated in various pathological manifestations of sialidosis and neurodegeneration. Thus, it is a novel therapeutic target for neurodegenerative changes in the Alzheimer's brain. However, to manipulate NEU1 as a therapeutic target, it is imperative to understand that, although NEU1 is commonly known for its lysosomal catabolic function, it is also involved in other pathways. NEU1 is involved in immune response modulation, elastic fiber assembly modulation, insulin signaling, and cell proliferation. In recent years, our knowledge of NEU1 has continued to grow, yet, at the present moment, current data is still limited. In addition, the unique biochemical properties of NEU1 make it challenging to target it as an effective therapeutic option for sialidosis, which is a rare disease but has an enormous patient burden. However, the fact that NEU1 has been linked to the pathology of Alzheimer's disease, which is rapidly growing worldwide, makes it more relevant to be studied and explored. In the present study, the authors have discussed various cellular mechanisms involving NEU1 and how they are relevant to sialidosis and Alzheimer's disease.

Pre-conceptional and prenatal exposure to pesticides and pediatric neuroblastoma. A meta-analysis of nine studies.

Neuroblastoma is primarily an embryonal tumor of infancy. Recently, some toxicological agents used as pesticides have been associated with an increased incidence of this tumor. We intended to determine the potential association between prenatal exposure to pesticides and the incidence of neuroblastoma in children. Studies targeting the link between neuroblastoma and pesticides were searched in PUBMED, SCOPUS, and Google Scholar from January 1, 1960, through December 2020. We performed a PRISMA-based systematic review and meta-analysis. In addition, we took into consideration the IARC evaluation on pesticides issued in recent monographs. Prenatal pesticide exposure is associated with an increased risk of neuroblastoma with an OR of 1.6 (1.1-2.3; p = 0.013), while the OR is 1.0 (0.8-1.3; p = 0.723) for pesticide exposure after birth. There is a significant association between prenatal pesticide exposure and neuroblastoma. We emphasize the IARC conclusions evaluating the carcinogenicity of diazinon, glyphosate, malathion, parathion, and tetrachlorvinphos.

Parental Pesticide Exposure and Childhood Brain Cancer: A Systematic Review and Meta-Analysis Confirming the IARC/WHO Monographs on Some Organophosphate Insecticides and Herbicides.

BACKGROUND: Brain tumors are the second most common neoplasm in the pediatric age. Pesticides may play an etiologic role, but literature results are conflicting. This review provides a systematic overview, meta-analysis, and IARC/WHO consideration of data on parental exposure to pesticides and childhood brain tumors. METHODS: We searched PubMed, SCOPUS, and Google Scholar for literature (1 January 1966-31 December 2020) that assessed childhood brain tumors and parental exposure to pesticides. We undertook a meta-analysis addressing prenatal exposure, exposure after birth, occupational exposure, and residential exposure. A total of 130 case-control investigations involving 43,598 individuals (18,198 cases and 25,400 controls) were included. RESULTS: Prenatal exposure is associated with childhood brain tumors (odds ratio, OR = 1.32; 95% CI: 1.17-1.49; I2 = 41.1%). The same occurs after birth exposure (OR = 1.22; 95% CI: 1.03-1.45, I2 = 72.3%) and residential exposure to pesticides (OR = 1.31; 95% CI: 1.11-1.54, I2 = 67.2%). Parental occupational exposure is only marginally associated with CBT (OR = 1.17, 95% CI: 0.99-1.38, I2 = 67.0%). CONCLUSIONS: There is an association between CBT and parental pesticides exposure before childbirth, after birth, and residential exposure. It is in line with the IARC Monograph evaluating the carcinogenicity of diazinon, glyphosate, malathion, parathion, and tetrachlorvinphos.

Therapeutic Potential of Neu1 in Alzheimer's Disease Via the Immune System.

Alzheimer's Disease (AD) is pathologically characterized by the accumulation of soluble oligomers causing extracellular beta-amyloid deposits in form of neuritic plaques and tau-containing intraneuronal neurofibrillary tangles in brain. One proposed mechanism explaining the formation of these proteins is impaired phagocytosis by microglia/macrophages resulting in defective clearance of soluble oligomers of beta-amyloid stimulating aggregation of amyloid plaques subsequently causing AD. However, research indicates that activating macrophages in M2 state may reduce toxic oligomers. NEU1 mutation is associated with a rare disease, sialidosis. NEU1 deficiency may also cause AD-like amyloidogenic process. Amyloid plaques have successfully been reduced using NEU1.Thus, NEU1 is suggested to have therapeutic potential for AD, with lysosomal exocytosis being suggested as underlying mechanism. Studies however demonstrate that NEU1 may activate macrophages in M2 state, which as noted earlier, is crucial to reducing toxic oligomers. In this review, authors discuss the potential therapeutic role of NEU1 in AD via immune system.

SAMHD1 as the Potential Link Between SARS-CoV-2 Infection and Neurological Complications.

The recent pandemic of coronavirus infectious illness 2019 (COVID19) triggered by SARS-CoV-2 has rapidly spread around the globe, generating in severe events an acute, highly lethal pneumonia and death. In the past two hitherto similar CoVs, the severe acute respiratory syndrome CoV (SARS-CoV-1) and Middle East respiratory syndrome CoV (MERS-CoV) also gained universal attention as they produced clinical symptoms similar to those of SARS-CoV-2 utilizing angiotensin-converting enzyme 2 (ACE2) receptor and dipeptidyl peptidase 4 (DPP4) to go into the cells. COVID-19 may also present with overtly neurological symptoms. The proper understanding of the expression and dissemination of ACE2 in central and peripheral nerve systems is crucial to understand better the neurological morbidity caused by COVID-19. Using the STRING bioinformatic tool and references through text mining tools associated to Coronaviruses, we identified SAMHD1 as the probable link to neurological symptoms. Paralleled to the response to influenza A virus and, specifically, respiratory syncytial virus, SARS-CoV-2 evokes a response that needs robust induction of a subclass of cytokines, including the Type I and, obviously, Type III interferons as well as a few chemokines. We correlate ACE2 to the pathogenesis and neurologic complications of COVID-19 and found that SAMHD1 links to NF-κB pathway. No correlation was found with other molecules associated with Coronavirus infection, including ADAR, BST2, IRF3, IFITM3, ISG15, MX1, MX2, RNASEL, RSAD2, and VPRBP. We suggest that SAMHD1 is the molecule that may be behind the mechanisms of the neurological complications associated with COVID-19.

Association between factor V Leiden mutation and recurrent pregnancy loss in the middle east countries: a Newcastle-Ottawa meta-analysis.

PURPOSE: Heritable thrombophilia is a category of genetic disorders of the coagulation cascade with the increasing risk of thrombus formation and recurrent pregnancy loss (RPL). Factor V Leiden (FVL) (R506Q) mutation is the most common genetic cause of deep venous thrombosis, but its association with RPL has been inconsistent in studies arising from non-Western countries. The present metanalysis was aimed to determine whether an association exists between FVL and RPL in the Middle East. METHODS: We searched PubMed, MEDLINE Web of Science, Scopus, and Embase, evaluating the association between the FVL and RPL. The Middle East countries (Bahrain, Cyprus, Egypt, Iran, Iraq, Israel, Jordan, Kuwait, Lebanon, Oman, Qatar, Saudi Arabia, The State  of Palestine, Syria, Turkey, The United Arab Emirates, and Yemen) were evaluated in succession. Raw data were extracted, and 19 case-control studies were included in our final analysis. RESULTS: Overall, 2513 cases and 1836 controls in the Middle East showed a prevalence of FVL mutation as 12.6% and 4.9% in patients and controls, respectively. To evaluate the relationship between FVL mutation and RPL, we used Forest plot (random effect model) with the overall random OR of 2.37 (CI 95%: 1.50-3.75). FVL mutation was associated with a higher risk of RPL. In Iran, the OR was 1.90 (95% CI 1.04-3.45), and in Turkey, the OR was 3.01 (95% CI 1.10-8.23). CONCLUSION: The results of our study support an association between FVL mutation status and RPL in women of the Middle East countries. It is recommended that specific policies include comprehensive testing for FVL mutation as a standard of care in women of the Middle East region with unexplained RPL.

Sialidosis: A Review of Morphology and Molecular Biology of a Rare Pediatric Disorder.

Sialidosis (MIM 256550) is a rare, autosomal recessive inherited disorder, caused by α-N-acetyl neuraminidase deficiency resulting from a mutation in the neuraminidase gene (NEU1), located on 6p21.33. This genetic alteration leads to abnormal intracellular accumulation as well as urinary excretion of sialyloligosaccharides. A definitive diagnosis is made after the identification of a mutation in the NEU1 gene. So far, 40 mutations of NEU1 have been reported. An association exists between the impact of the individual mutations and the severity of clinical presentation of sialidosis. According to the clinical symptoms, sialidosis has been divided into two subtypes with different ages of onset and severity, including sialidosis type I (normomorphic or mild form) and sialidosis type II (dysmorphic or severe form). Sialidosis II is further subdivided into (i) congenital; (ii) infantile; and (iii) juvenile. Despite being uncommon, sialidosis has enormous clinical relevance due to its debilitating character. A complete understanding of the underlying pathology remains a challenge, which in turn limits the development of effective therapeutic strategies. Furthermore, in the last few years, some atypical cases of sialidosis have been reported as well. We herein attempt to combine and discuss the underlying molecular biology, the clinical features, and the morphological patterns of sialidosis type I and II.